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Poisoning Conference β Answer Key
Built from GI Lecture 21 (LOs 1β12). Companion to gi21_active_recall.html.
π Use alongside: GI Lecture 21 β Poisoning Conference
Focus on: NPDS epidemiology, poisoned-patient approach (history/exam/labs), toxidromes, specific agents (APAP, salicylates, iron, TCA, opioids, CO, toxic alcohols), decontamination, enhanced elimination, and antidotes.
Epi & Approach
Labs & Toxidromes
Decon & Elimination
APAP / Salicylates / Iron
TCA / Opioid / CO / Alcohols
Antidotes & Pearls
Practice Qs
LO 1 Β· LO 2 Β· LO 3
ON EXAM β NPDS top killers (SOAP), history framework (WARS), vital sign extremes, alert presentations that demand immediate intervention
NPDS β top causes of poisoning deaths (SOAP)
S Sedatives/hypnotics (benzos, sleep aids)
O Opioids (prescription + illicit, fentanyl surge)
A Acetaminophen (APAP β #1 acute liver failure)
P Poisons (illicit drugs, pesticides, industrial chemicals)
Epidemiology β age + intent
Peak pediatric unintentional age 1β3 years ("exploratory ingestion")
Most common adolescent/adult intent Intentional (self-harm/suicide attempt)
Most common route overall Oral ingestion
History framework β WARS
Letter Stands For Example Question W WHAT was taken? (substance ID, bottle inventory) Name, strength, count remaining? A AMOUNT β how much? (max possible) Count empty bottles/missing pills; max dose R ROUTE + timing Oral, IV, inhalation; time since ingestion S SYMPTOMS / SIGNS developed AMS, vomiting, seizures, abnormal vitals
Vital-sign extremes
Vital Finding Classic Toxin Category Hypotension + bradycardia Ξ²-blockers, CCBs, digoxin, clonidine, opioids Hypertension + tachycardia Sympathomimetics (cocaine, amphetamines, PCP), anticholinergics Hyperthermia Sympathomimetics, serotonin syndrome, NMS, salicylates, anticholinergics Hypothermia Sedatives (benzos, barbs, opioids), ethanol Bradypnea + miosis + coma Opioid toxidrome
Red-flag alert presentations
AMS + focal neuro findings Structural cause (stroke, bleed, mass) β image the head; NOT pure tox
Seizures in overdose β top 2 TCAs, INH (isoniazid); also cocaine, tramadol, bupropion
Wide-complex tachycardia TCA (Na channel blocker) β terminal R in aVR
Cyanosis unresponsive to Oβ Methemoglobinemia, sulfhemoglobinemia (abnormal Hb)
Cherry-red skin + normal SpOβ Carbon monoxide (CO) poisoning
LO 4 Β· LO 5 Β· LO 12
ON EXAM β anion gap MUDPILES, osmolar gap toxins, UDS false pos/neg, co-oximetry, 4 classic toxidromes
MUDPILES β anion gap metabolic acidosis
Letter Toxin M Methanol, Metformin U Uremia D DKA / Alcoholic/Starvation ketoacidosis P Propylene glycol / Paraldehyde I Iron, Isoniazid (INH), Ibuprofen L Lactic acidosis (shock, CO, CN, metformin) E Ethylene glycol S Salicylates
Osmolar gap
Suspicious cutoff >25 mOsm/kg (especially >50)
3 toxic alcohols raising osmol gap Methanol, Ethylene glycol, Isopropanol (+ propylene glycol)
Large osmol gap, NO anion gap Isopropanol (β acetone; ketosis without acidosis)
UDS limitations
Never rule out poisoning with a negative UDS β many opioids and synthetics are missed.
False NEG opioids Fentanyl, methadone, oxycodone, tramadol, buprenorphine (synthetic/semi-synthetic)
False POS benzo Sertraline, oxaprozin (NSAID), rifampin
False POS amphetamine Pseudoephedrine, phenylephrine, bupropion, selegiline, labetalol
Positive = active intox? No β detects metabolites for days to weeks; cannot time exposure
Toxidrome comparison
Feature Anticholinergic Cholinergic Sympathomimetic Opioid Mental status Agitated delirium Confusion/coma/seizures Agitation/psychosis CNS depression/coma Pupils Mydriasis Miosis Mydriasis Miosis Skin Hot, DRY, flushed WET (diaphoresis/SLUD) Hot, diaphoretic Cool, pale/normal Bowel sounds Absent (ileus) Hyperactive Normal/increased Decreased Temperature Hyperthermia Normal Hyperthermia (severe) Normal/hypothermia Antidote Physostigmine (severe) Atropine + 2-PAM Benzos (supportive) Naloxone
Anticholinergic mnemonic
"Hot as a hare" Hyperthermia (anhydrosis)
"Dry as a bone" Dry skin and mucous membranes
"Red as a beet" Cutaneous vasodilation (flushing)
"Mad as a hatter" Agitated delirium (AMS/psychosis)
Cholinergic mnemonics
SLUDGE Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis
DUMBELS Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia, Emesis, Lacrimation, Salivation
Nicotinic findings Muscle fasciculations/weakness/paralysis; tachycardia + HTN (paradoxical); mydriasis
LO 6 Β· LO 7
ON EXAM β activated charcoal, MDAC (CPSA), urinary alkalinization, hemodialysis (SLIME), WBI
Activated charcoal basics
Adult dose 1 g/kg PO (or 25β100 g)
Window Within 1 hour of ingestion (best)
Airway CI Unprotected airway / depressed LOC without intubation (aspiration)
GI CI Ileus, obstruction, caustics, GI perforation
LAME Ca β charcoal misses
Letter Substance L Lithium A Alcohols (ethanol, methanol, EG, isopropanol) M Metals (iron, lead, mercury, arsenic) E Electrolytes (Na, K, Mg) Ca Caustics (acids/alkalis) β can worsen injury
MDAC β CPSA indications
Letter Drug Reason C Carbamazepine Enterohepatic recirculation P Phenobarbital Enterohepatic recirc + slow clearance S Salicylates (severe/ER) Prevents resorption from concretions A Aminophylline / Theophylline Enterohepatic + narrow window
Urinary alkalinization
Agent Sodium bicarbonate infusion
Target urine pH >7.5 (ideally 7.5β8)
Principle Ion trapping β ionizes weak acids in alkaline urine, prevents reabsorption
Classic toxin #1 Salicylates
Classic toxin #2 Phenobarbital
Electrolyte to monitor Potassium β hypokalemia blocks alkalinization (aldosterone exchanges K for H)
SLIME β HD-removable toxins
Letter Toxin S Salicylates L Lithium I Isopropanol M Methanol + Metformin (lactic acidosis) E Ethylene glycol
Dialyzability criteria
Protein binding Low (<50%)
Whole-bowel irrigation
Agent Polyethylene glycol (PEG), 1.5β2 L/hr until effluent clear
Indication #1 Iron (radiopaque tablets; charcoal doesn't bind)
Indication #2 Sustained-release / enteric-coated (verapamil SR, lithium SR)
Indication #3 Body packers (cocaine, heroin packets)
LO 8 Β· LO 9
ON EXAM β APAP 4 phases + NAPQI, nomogram + NAC; salicylate mixed acid-base + tinnitus; iron 5 phases + "quiet phase" trap
APAP β 4 phases
Phase Time Features 1 0β24 hr Asymptomatic OR nausea/vomiting/malaise; NO lab abnormalities 2 24β72 hr RUQ pain, βAST/ALT/INR; "feels better" but labs worsening 3 72β96 hr Peak hepatotoxicity β fulminant liver failure, encephalopathy, coagulopathy, acidosis 4 4 days β 2 weeks Recovery OR death from liver failure
APAP mechanism
Toxic metabolite NAPQI (N-acetyl-p-benzoquinone imine)
Neutralizing molecule Glutathione (GSH) β depleted in overdose
Tissue injured Liver (centrilobular / zone 3 necrosis)
APAP labs + antidote
Level timing 4 hours post-ingestion (plot on nomogram)
Nomogram axes APAP level vs time since ingestion (Rumack-Matthew)
Antidote + MOA N-acetylcysteine (NAC) β glutathione precursor + direct NAPQI binding
Window Within 8β10 hours most effective; give even if late/uncertain timing
Salicylates β clinical + labs
Early ear symptom Tinnitus (classic)
Respiratory pattern Tachypnea/hyperpnea (direct medullary stim β resp alkalosis)
Acid-base Primary respiratory alkalosis + primary anion-gap metabolic acidosis (MIXED)
Temperature Hyperthermia β uncouples oxidative phosphorylation β heat, not ATP
Severe finding Cerebral edema, ARDS (non-cardiogenic pulmonary edema), seizures, coma
Salicylate treatment
Alkalinization rationale Ion trapping β keeps drug ionized in urine + shifts out of CNS
Serum pH target ~7.5 (alkalemia drives drug from brain)
HD cutoff >100 mg/dL acute (or >60 mg/dL chronic); severe acidosis, AMS, renal failure, pulmonary edema
Avoid intubation why Sedation/paralysis abolishes compensatory hyperventilation β sudden severe acidemia β death
Iron β 5 phases
Phase Time Hallmark 1 GI 30 min β 6 hr Vomiting, diarrhea, hematemesis, abdominal pain 2 "Quiet" 6β24 hr Symptoms improve but cellular injury ongoing (TRAP!) 3 Shock 6β48 hr Shock, anion-gap acidosis, coagulopathy, multi-organ failure 4 Hepatic 12β96 hr Elevated LFTs, coagulopathy 5 Delayed 2β8 weeks GI strictures/obstruction from mucosal scarring
Iron β antidote + diagnostics
Antidote + MOA Deferoxamine β chelates free iron, renally excreted
Urine color "Vin rosΓ©" (pinkish/red) β indicates chelated iron excretion
Imaging Abdominal X-ray β iron tablets are radiopaque
WBI use Large ingestions (tablets visible on X-ray; charcoal doesn't bind)
LO 8 Β· LO 9
ON EXAM β TCA 3 receptor effects + QRS + NaHCOβ; naloxone; CO cherry red + co-oximetry; methanol vs EG; fomepizole
TCA β 3 receptor effects
Receptor Effect Fast NaβΊ channels Slowed cardiac conduction β wide QRS, R in aVR, VT/VF Muscarinic (M1) Anticholinergic β mydriasis, dry skin, tachy, ileus, delirium Ξ±β-adrenergic Hypotension (vasodilation), reflex tachycardia
TCA β EKG + treatment
EKG finding Terminal R wave in aVR >3 mm; QRS widening; right axis deviation
QRS threshold >100 ms β seizure risk; >160 ms β arrhythmia risk
Antidote MOA NaHCOβ IV β alkalemia βbinding to Na channel + Na load overcomes block
Avoid flumazenil why Precipitates seizures + unmasks TCA cardiotox; benzos are protective vs TCA seizures
Opioid
Classic triad CNS depression + respiratory depression (bradypnea) + miosis
Antidote + route Naloxone β IV/IM/intranasal/SC
Duration issue Naloxone tΒ½ 30β90 min, MUCH shorter than most opioids β re-dose or infusion to prevent re-sedation
QT prolongation opioid Methadone (and loperamide in massive OD) β torsades
Seizure opioid Meperidine (normeperidine metabolite); tramadol
Withdrawal risk Chronic users β use lowest effective naloxone dose (0.04β0.4 mg)
CO
Hb affinity ~200β240Γ greater than Oβ β functional anemia
Mitochondrial target Cytochrome c oxidase (complex IV) β lactic acidosis
Why SpOβ fails Pulse ox cannot distinguish CO-Hb from Oβ-Hb (similar absorption at 660/940 nm)
Test of choice Co-oximetry (arterial/venous carboxyhemoglobin level)
First-line Rx 100% Oβ via non-rebreather (CO-Hb tΒ½ 4β5h β 80 min)
HBO indications LOC/syncope, neurologic symptoms, pregnancy, CO-Hb >25%, cardiac ischemia, severe acidosis
Pregnancy level >15% (fetal Hb binds CO more tightly; fetal CO-Hb lags maternal)
Methanol vs Ethylene Glycol
Feature Methanol Ethylene Glycol Source Wood alcohol, antifreeze, moonshine, washer fluid Antifreeze (sweet), coolants, deicers Toxic metabolite Formaldehyde β formic acid Glycolate β oxalate Organ Retina/optic nerve β "snowstorm" blindness Kidneys (ATN from Ca-oxalate) Distinctive Visual changes/blindness, putaminal lesions (MRI) Ca-oxalate crystalluria, AKI, hypocalcemia UA clue Usually unremarkable Ca-oxalate crystals; may fluoresce under Wood lamp
Toxic alcohol treatment
First-line antidote Fomepizole (4-methylpyrazole, 4-MP)
Enzyme blocked Alcohol dehydrogenase (ADH)
Backup Ethanol infusion (competes with ADH; harder to dose)
HD role Removes parent alcohol + toxic metabolites; for severe acidosis, high levels, end-organ damage
Methanol cofactor Folate/folinic acid (accelerates formate breakdown)
EG cofactor Pyridoxine (B6) β shunts glyoxylate to glycine (+ thiamine)
LO 10 Β· LO 11
ON EXAM β antidote master table, delayed-toxicity agents, supportive care
Antidote master table
Toxin Antidote Acetaminophen N-acetylcysteine (NAC) Opioids Naloxone Benzodiazepines Flumazenil (rarely used β seizure risk) Iron Deferoxamine TCA (cardiac) Sodium bicarbonate Salicylates NaHCOβ (urinary alkalinization) + HD Methanol / EG Fomepizole (or ethanol) + folate (MeOH) or pyridoxine/thiamine (EG) Carbon monoxide 100% Oβ / hyperbaric Oβ Cyanide Hydroxocobalamin OR Na thiosulfate + Na nitrite Methemoglobinemia Methylene blue Organophosphates Atropine + Pralidoxime (2-PAM) Anticholinergic (severe) Physostigmine (avoid in TCA coingestion) Ξ²-blocker Glucagon + high-dose insulin + Ca + lipid Calcium channel blocker Calcium + high-dose insulin + glucagon + vasopressors Digoxin Digoxin-specific Fab (DigiFab) Heparin Protamine sulfate Warfarin Vitamin K + FFP/PCC (acute) Lead (severe) Succimer (DMSA); CaNaβ-EDTA + BAL for encephalopathy INH overdose (seizures) Pyridoxine (B6), high-dose
Delayed-toxicity trap
Agent Delay Why APAP ~24 hr (phase 1 asymptomatic) Glutathione depletion + NAPQI damage accumulate slowly Iron (phase 2) 6β24 hr GI symptoms improve; ongoing mitochondrial injury β shock later SR opioid Hours β depot release Extended-release matrix slowly releases drug Methanol / EG 8β24 hr Parent alcohol nontoxic until metabolized (formate, oxalate) Warfarin 48β72 hr Factor II (tΒ½ 60h) must deplete before INR rises
Rapid-onset toxicity
Agent Time-to-lethality Key Intervention Cyanide Minutes Hydroxocobalamin IV immediately OP (large exposure) Minutes to hours Atropine titrated to dry secretions + 2-PAM + airway TCA massive OD Hours NaHCOβ + airway + benzos for seizures CCB Hours (refractory shock) Ca + HD insulin + glucagon + vasopressors
Supportive care priorities
First priority ABCs β airway, breathing, circulation (+ decon of skin/eyes if topical)
Empiric agents in AMS Dextrose + thiamine + naloxone ("coma cocktail"; Oβ first)
Thiamine before dextrose Prevents precipitating Wernicke encephalopathy in alcohol-dependent/malnourished
Intubation GCS GCS β€8 (or failure to protect airway, vomiting + AMS, refractory hypoxia)
Seizures + hyperthermia
First-line seizure Benzodiazepines (lorazepam, diazepam, midazolam)
Avoid which anticonvulsant Phenytoin β ineffective/harmful in TCA, INH, theophylline
Hyperthermia Rx Aggressive cooling (ice, evap) + benzos (βadrenergic/serotonin tone) + fluids
Avoid for tox hyperthermia Antipyretics (APAP, NSAIDs) β ineffective (not hypothalamic set-point fever)
Practice Questions
Q1: APAP overdose timing
A 22-year-old woman arrives 6 hours after ingesting ~30 extra-strength acetaminophen tablets. Currently asymptomatic. BEST next step?
B β Draw 4-hour level + plot on Rumack-Matthew nomogram; start NAC if above treatment line. Phase 1 is classically asymptomatic β normal exam does NOT rule out toxicity. NAC most effective within 8 hours. If timing uncertain or level above line, start NAC empirically.
Q2: Mixed acid-base
45yo M tachypneic with tinnitus, AMS, vomiting. pH 7.48, pCOβ 22, HCOβ 16, AG 22. Diagnosis?
C β Salicylates. Classic: primary respiratory alkalosis (medullary stim β tachypnea) + AG metabolic acidosis (uncoupling oxphos β lactate/ketones). Tinnitus = pathognomonic. Treat with NaHCOβ for urine/serum alkalinization; HD if >100 mg/dL, AMS, renal failure, pulmonary edema.
Q3: Wide-complex tachycardia
30yo F suicide attempt. Somnolent, tachy, hypotensive, dry warm skin, mydriasis. QRS 130 ms + terminal R in aVR. Treatment?
B β Sodium bicarbonate IV. TCA toxicity (anticholinergic + Na-channel block). NaHCOβ: (1) alkalemia reduces drug binding to Na channel, (2) Na load overcomes block. Flumazenil is CONTRAindicated. QRS >100 ms = seizure risk; >160 ms = arrhythmia risk.
Q4: HD indications
Which toxin is MOST effectively removed by HD?
C β Lithium. SLIME β Salicylates, Lithium, Isopropanol, Methanol/Metformin, Ethylene glycol. Dialyzable: low MW, low protein binding, low Vd, water soluble. Lithium meets all. Dig/TCA/CCB all have huge Vd.
Q5: Cherry-red skin
Family of 4 obtunded in winter home with faulty furnace. SpOβ 99% but cherry-red mucosa + lactic acidosis. Confirmatory test?
C β Co-oximetry (CO-Hb level). Standard pulse ox CANNOT distinguish CO-Hb from Oβ-Hb. PaOβ is normal (dissolved Oβ unchanged). HBO: severe CNS sx, LOC, pregnancy, CO-Hb >25% (>15% if pregnant).
Q6: Toxic alcohol
52yo M intoxicated, no alcohol smell. AG 28, osmolar gap 25. Ca-oxalate crystals on UA. Treatment?
B β Fomepizole IV. Ethylene glycol poisoning. Fomepizole = competitive ADH inhibitor; prevents toxic metabolite formation. Ethanol = backup. Thiamine + pyridoxine shunt to non-toxic metabolites. HD for severe acidosis/renal failure/high levels.
Q7: Charcoal CI
Charcoal is LEAST effective for which ingestion?
D β Lithium. LAME Ca β Lithium, Alcohols, Metals (iron), Electrolytes, Caustics β not adsorbed. Lithium is an ion; WBI preferred (especially SR).
Q8: Cholinergic crisis
40yo farmworker sprayed with pesticide. Copious secretions, miosis, bradycardia, bronchoconstriction, fasciculations. First-line?
A β Atropine IV titrated to dry pulmonary secretions. OP poisoning (AChE inhibition) = cholinergic crisis. Atropine titrated to DRY SECRETIONS (not HR/pupils). Give pralidoxime WITH atropine (not alone) within 24β48h before "aging." Physostigmine would worsen cholinergic excess.